Modulation of Akt kinase activity by ubiquitination
| Project/Area Number |
22370046
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Functional biochemistry
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| Research Institution | Hokkaido University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SUIDU Futoshi 北海道大学, 遺伝子病制御研究所, 講師 (90431379)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥18,980,000 (Direct Cost: ¥14,600,000、Indirect Cost: ¥4,380,000)
Fiscal Year 2012: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2011: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2010: ¥9,100,000 (Direct Cost: ¥7,000,000、Indirect Cost: ¥2,100,000)
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| Keywords | AKT / 蛋白分解 / ＮＳ１ / ＴＣＬ１ｂ / シグナル伝達 / Akt |
|---|
| Research Abstract |
Serine threonine Akt is a core intra-cellular survival regulator. In this study, we demonstrated that the functional interaction of NS1 with Akt and clarified that the functional importance of influenza virus NS1 with Akt in biocmical analysis. The results together supported the functional importance of influenza virus NS1 with Akt.We clarified that TCL1b functions as an Akt kinase co-activator and exhibitsoncogenicity both in vitro and in vivo using biochemical analysis, bioinformatics, and generation of TCL1b transgenic mice which resulted in angiosarcoma. By immunohistochemistry, most of human angiosarcoma samples and various cancer tissues were positively stained by both anti-TCL1b and anti-phospho-Akt antibodies. Moreover,TCL1b structure-based inhibitor “TCL1b-Akt-in” inhibited Akt kinase activity, hence, suppressed cellular proliferation of sarcoma. The current study disclosed TCL1b bears oncogenicity, and hence serves as a novel therapeutic target for human neoplasticdiseases.
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Report
(4 results)
Research Products
(43 results)
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[Journal Article] Dendritic cell-derived TNF-αisresponsible for development of IL-10- producing CD4+ T cells2010
Author(s)
N.Hirata,Y.Yanagawa,M.Satoh,H.Ogura,T.Ebihara,M.Noguchi,M.Matsumoto,H.To gashi,T.Seya, K.Onoe,K.Iwabuchi
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Journal Title
Cell Immunol.
Volume: 261
Pages: 37-4
NAID
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Peer Reviewed
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[Presentation] ユビキチン化によるAKT活性の調節メカニズムの解析2010
Author(s)
F. Suizu,Y. Hiramuki,F. Okumura,M. Matsuda,A. Okumura,N. Hirata,M. Narita,T. Kohono,J. Yokota,M. Bohgaki,C. Obuse,S. Hatakeyama T. Obata,M Noguchi
Organizer
第33回日本分子生物学会
Place of Presentation
神戸市・神戸ポートアイランド
Related Report
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